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PHYS - REPRO > 3. HPG AXIS II > Flashcards

3. HPG AXIS II Flashcards

1
Q

Define puberty

A

Puberty refers to the change from the non-reproductive state to the reproductive state. It involves the gonads producing mature gametes
- Puberty is characterised by two endocrinological events

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2
Q

What are the two endocrine events of puberty?

A
  1. Adrenarche (pubarche)

2. Gonadarche

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3
Q

What is adrenarche?

A
  • Adrenarche is the first endocrine event of puberty, it’s characterized by cellular remodeling of the adrenal gland resulting in changes in adrenal androgen secretion particularly DHEA & DHEAS (dehydro-epiandersterone)
  • Adrenal androgens are released from the zona reticularis of the adrenal cortex
  • Adrenarche causes adrenal androgen levels to increase at between 6-8 years. there’s a peak in the mid 20s where there’s a 20 fold increase
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4
Q

Describe the cellular remodeling of the adrenal gland

A
  • The adrenal gland is split into two zones:
    1. Foetal zone
    2. Definitive zone
  • During foetal development, the foetal zone is responsible for androgen secretion
  • After birth, the foetal layer shrinks & the definitive layers differentiates into layers producing the adrenal androgens during adrenarche
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5
Q

What is pubarche?

A
  • Pubarche occurs as a result of adrenarche
  • Pubarche refers to the growth of pubic or axillary hair as a result of adrenal androgen secretion
  • It’s also associated with increased sebum production, which can lead to acne & infection
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6
Q

What is gonadarche?

A
  • Gonadarche is the second endocrine event of puberty. It refers to re-activation of the HPG axis at around 11 years, occurring many years after adrenarche
  • The HPG axis is turned on at around the 16th gestational week where the gender of an embryo can be determined. It continues to remain active until 1-2 years of age when it’s switched off
  • The re-activation of the HPG axis at 11 years leads to GnRH secretion leading to gonadal steroid production & gamete production = fertility
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7
Q

Describe the release of GnRH during pubertal development?

A
  • During gonadarche, the re-activation of the HPG axis leads to GnRH secretion
  • Initially, there’s a nocturnal rise in GnRH secretion during early puberty
  • GnRH secretions continue to rise until they become consistent up until adulthood/late puberty
  • GnRH levels cannot be measured because it’s a hypothalamic hormone, but studies have measured LH levels as a pulse of GnRH produces a pulse of LH
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8
Q

What stimulates the onset of puberty?

A

Puberty is a maturational event which involves the influence of:

  1. Maturation GnRH neurones which produce GnRH stimulating the HPG axis
  2. Environmental factors including body fat
  3. Kisspeptin
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9
Q

Describe the relationship between body fat & reproduction/puberty?

A
  • There’s a proposed link between body fat & metabolism
  • Individuals with anorexia nervosa or those who do intensive training:
    1. Reduced response to GnRH = impaired gonadotrophin levels
    2. Amenorrhea
  • Studies have shown that at least 17% body fat is needed for menarche & 22% for fertilisation/pregnancy
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10
Q

How are ghrelin & leptin involved in the HPG axis?

A
  • Ghrelin & leptin are involved in feeding behaviour

- They act on the hypothalamus to cause feedback to kisspeptin which can affect pubertal onset

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11
Q

What do inactivating mutations of Kisspeptin or it’s receptor lead to?

A
  • INACTIVATING MUTATIONS of Kisspeptin receptor (KISS1R) or the gene coding for kisspeptin can lead to hypogonadism & a failure to enter puberty. Both of which are characteristic of hypogonadotropic hypogonadism
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12
Q

*What do activating mutations of Kisspeptin or it’s receptor lead to?

A
  • ACTIVATING MUTATIONS of the kisspeptin receptor can mean that it’s active even when there’s no kisspeptin
  • This can lead to precocious puberty, the receptor is active in the absence of kisspeptin so the downstream signalling is also activated
  • It activates gonadal function without gonadarche & without the activation of the HPG axis (Gonadotrophin independent precocious puberty - loss of consonance)
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13
Q

Define consonance in regards to puberty

A
  • Consonance refers to the progression of the changes in puberty in order
  • the pace, duration, age of onset may differ between individuals but the order must be the same
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14
Q

What three things do the Tanner stages of development measure?

A
  • The Tanner stages measure physical pubertal development on a scale with 5 stages
  • It measures:
    1. Pubic & axillary hair growth
    2. Breast development (thelarche)
    3. Penile length & testicular volume
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15
Q

What 8 physical changes occur in girls in puberty?

A
  1. Thelarche - first outward sign of oestrogen
  2. Pubic & axillary hair growth
  3. Uterus enlarges, cell cytology changes due to oestrogen
  4. Uterine tubes, cervical & vaginal changes
  5. Height
  6. Body shape
  7. Increase in ovarian size 7 follicular growth
  8. Menarche
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16
Q

What is menarche?

A
  • Menarche refers to the occurrence of the first menstrual period
17
Q

Describe the onset of fertility in girls?

A
  • Fertility doesn’t occur until after a year after menarche

- Menarche doesn’t mark fertility, because the cycles are irregular as the HPG axis is still priming

18
Q

What are 8 physical changes that occur in boys during puberty?

A
  1. Development of external genitalia - increase in testicular volume to > 4ml, growth of penis, scrotum
  2. Lumen of vas deferens enlarge
  3. Seminal vesicles & prostate develop
  4. Facial hair
  5. Pubic & axillary hair growth
  6. Larynx changes - androgens enlarge larynx leading to deepening of voice
  7. Height
  8. Body shape
19
Q

Describe the onset of fertility in boys

A
  • The onset of fertility in boys is immediate with boys being fertile at the beginning of puberty unlike females
20
Q

What two hormones interact to cause a growth spurt & how?

A
  1. GROWTH HORMONE
  2. OESTROGEN
    - there’s a BIPHASIC EFEFCT of oestrogen on epiphyseal bone growth (two phases)
  3. Low oestrogen - stimulates linear growth & bone maturation
  4. High oestrogen -epiphyseal maturation, marks the end of growth spurt
21
Q

What are the two types of pilosebaceous units & the effect of androgens?

A
  • Adrenal androgens act on Pilosebaceous units to cause increased sebum or hair growth
    1. SEBACEOUS PCU = increase in sebum production
    2. VELLUS PCU - responsible for hair growth, TERMINAL PCU & APO-PCU
22
Q

What are the two types of Vellus PCU & what hair growth do they cause?

A
  1. TERMINAL PCU - responsible for facial hair growth

2. APO-PCU - responsible for pubic & axillary hair growth

23
Q

What are 3 psychological changes associated with puberty?

A
  1. Development of sexual personality
  2. Increased sexual awareness
  3. Increased need for independence
24
Q

What is precocious puberty?

A
  • Precocious puberty refers to the early onset of puberty, it’s the development of secondary sexual characteristic before 8 in girls & 9 in boys
25
Q

What are the two types of precocious puberty?

A
  1. GONADOTROPHIN DEPENDENT PRECOCIOUS PUBERTY

2. GONADOTROPHIN INDEPENDENT PUBERTY

26
Q

What is gonadotrophin dependent precocious puberty?

A
  • GONADOTROPHIN DEPENDENT precocious puberty is known as central precocious puberty as t involves the HPG axis
  • It occurs due to issues with gonadotrophin secretion e.g
    1. Excess GnRH - leading to excess gonadotrophin
    2. Excess gonadotrophin - pituitary tumour
  • As it involves the HPG axis, gonadotrophin dependent precocious puberty has consonance
27
Q

What is gonadotrophin independent precocious puberty?

A
  • GONADOTROPHIN INDEPENDENT precocious puberty doesn’t involve the HPG axis
  • The hypothalamus & anterior pituitary are functioning normally but there’s premature gonadal maturation due to:
    1. Sex steroid secreting tumour
    2. Exogenous steroids
  • The gonads undergo maturation without activation of the HPG axis, without gonadarche
  • E.g KISSPEPTIN receptor activating mutations
  • There’s a loss of consonance in gonadotrophin independent precocious puberty
28
Q

Give two examples of Gonadotrophin independent precocious puberty?

A
  1. TESTOXICLOSIS

2. MCCUNE ALLBRIGHT SYNDROME

29
Q

What is testoxiclosis?

A
  • TESTOXICLOSIS is an activating mutation of the LH receptor on Leydig cells (males). This leads to the production of testosterone by Leydig cells resulting in enlarged male genitalia but no other physical changes
30
Q

*What is McCune Allbright syndrome?

A
  • McCune Allbright syndrome is caused by a mutation in the GNASI gene coding for the G alpha protein
  • The mutation leads to widespread activation of G-protein signalling including FSH, GnRH secretion causing precocious puberty
  • Adenylase cyclase goes into overdrive causing widespread activation of G-protein pathways, so it’s independent of gonadotrophins
  • Other symptoms include cafe au lait skin pigmentation, fibrous dysplasia
31
Q

Define pubertal delay

A
  • Pubertal delay refers to the absence of sexual maturation by 13 in girl & 14 in boys. It can also be the absence of menarche at 18 in girls
32
Q

What are the three types of pubertal delay?

A
  1. CONSTITUTIONAL PUBERTY - There’s a prolonged pre-pubertal phase, can be due to chronic diseases such as cystic fibrosis
  2. HYPOGONADOTROPIC HYPOGONADISM - Gonadal dysgenesis with Low FSH & LH
  3. HYOERGONADOTROPHIC GONADISM - Gonadal dysgenesis with high FSH, LH & low sex steroids. Impaired response of the gonads to gonadotrophins
33
Q

What is hypogonadotropic hypogonadism & give an example?

A
  • KALLMAN’S SYNDROME - A mutation in the KAL1 gene occurs. The KAL1 gene is responsible for the migration of GnRh neurones into the hypothalamus. The mutation leads to impaired GnRH migration & function therefore LOW FSH & LH
  • Also inactivating kisspeptin or kisspeptin receptor mutations
34
Q

Give an example of hypergonadotropic hypogonadism resulting from a normal karyotype

A
  • Hypergonadotropic hypogonadism = High FSH & LH with low gonadal steroids
  • NORMAL KARYOTYPE -= viral e.g mumps
35
Q

Give two examples of hypergonadotropic hypogonadism resulting from an abnormal karyotype?

A
  1. TURNER’S SYNDROME XO genotype, characterized by streak ovaries
  2. KLINEFELTER’S SYNDROME - XXY genotype with an extra Y

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